Stable Coronary Artery Disease Patients Research Articles

Impact of Direct Measurement of Small Dense Low-Density Lipoprotein Cholesterol for Long-Term Secondary Prevention in Patients with Stable Coronary Artery Disease.

This study investigated whether directly measured small dense low-density lipoprotein cholesterol (D-sdLDL-C) can predict long-term coronary artery disease (CAD) events compared with low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), apolipoprotein B (apoB), and estimated small dense low-density lipoprotein cholesterol (E-sdLDL-C) determined by the Sampson equation in patients with stable CAD. D-sdLDL-C measured at Showa University between 2010 and 2022, and E-sdLDL-C were evaluated in 790 male and 244 female patients with stable CAD. CAD events, defined as sudden cardiac death, onset of acute coronary syndrome, and/or need for coronary revascularization, were monitored for 12 years. Cutoff lipid levels were determined by receiver operating characteristic curves. CAD events were observed in 238 male and 67 female patients. The Kaplan-Meier event-free survival curves showed that patients with D-sdLDL-C ≥32.1 mg/dL (0.83 mmol/L) had an increased risk for CAD events (P = 0.007), whereas risk in patients with E-sdLDL-C ≥36.2 mg/dL (0.94 mmol/L) was not increased. In the group with high D-sdLDL-C, the multivariable-adjusted hazard ratio (HR) was 1.47 (95% CI, 1.15-1.89), and it remained significant after adjustment for LDL-C, non-HDL-C, or apoB and in patients treated with statins. HRs for high LDL-C, non-HDL-C, or apoB were not statistically significant after adjustment for high D-sdLDL-C. Higher D-sdLDL-C was associated with enhanced risk of high LDL-C, non-HDL-C, and apoB (HR 1.73; 95% CI, 1.27-2.37). Higher D-sdLDL-C can predict long-term recurrence of CAD in stable CAD patients independently of apoB and non-HDL-C. D-sdLDL-C is an independent risk enhancer for secondary CAD prevention, whereas E-sdLDL-C is not. UMIN-CTR Clinical Trial Number: UMIN000027504.

Novel prognostic impact and cell specific role of endocan in patients with coronary artery disease.

Both the clinical and mechanistic impacts of endocan were not well elucidated especially in coronary artery disease (CAD). This study aimed to investigate the prognostic and potential pathological role of endocan for cardiovascular (CV) events in stable CAD patients. A total of 1,071 stable CAD patients with previous percutaneous coronary intervention (PCI) were enrolled prospectively in a nationwide Biosignature study. Another cohort of 76 CAD patients with or without PCI were enrolled for validation. Baseline biomarkers including endocan level was measured and total CV events especially hard CV events (including CV mortality, non-fatal myocardial infection and stroke) during follow-up were identified. Circulating endothelial progenitor cells (EPCs) as an in vivo biological contributor to vascular repairment from CAD patients were used for the in vitro functional study. After 24months, there were 42 patients (3.92%) with hard CV events and 207 (19.3%) with total CV events in the study group. The incidence of both events was increased with the tertiles of baseline endocan level (hard events: 1.7%,3.4%, and 6.7% in 1st,2nd, and 3rd tertile respectively, p = 0.002; total events: 13.8%vs.16.2%vs.28.0%, p < 0.0001). Multivariate regression analysis revealed the independent association of endocan level with total and hard CV events. These findings were validated in another cohort with a 5-year follow-up. Furthermore, in vitro inhibition of endocan improved cell migration and tube formation capacities, and reduced cell adhesiveness of EPCs from CAD patients. Endocan might be a novel prognostic indicator, mechanistic mediator, and potential therapeutic target for clinical CAD.

C-36 | Association between coronary revascularization and reduction in ventricular arrhythmias in stable coronary artery disease patients: A systematic review and meta-analysis

C-36 | Association between coronary revascularization and reduction in ventricular arrhythmias in stable coronary artery disease patients: A systematic review and meta-analysis

The changes in health-related quality of life in stable coronary artery disease patients and intermediante coronary lesions after elective percutaneous coronary intervention

The aim – to analyze the factors, associated with the change in health-related quality of life (HRQoL) in stable coronary artery disease (SCAD) patients with intermediate coronary lesions at 3-months follow-up after elective percutaneous coronary intervention (PCI).Materials and methods. A prospective single-center study enrolled 84 SCAD patients (mean age 64±8 years; males – 73 %) with intermediate coronary lesions (stenosis 50-90 %) (by invasive coronary angiography [ICA]), consecutively enrolled and hospitalized with the aim of elective PCI to be performed. HRQoL was evaluated by SF-36 (physical health summary [PHsum] and mental health summary [МНsum]) and SAQ (Seattle Angina Questionnaire»; the domains «physical limitation» [PL], «angina stability» [AS], «angina frequency» [AF], «treatment satisfaction» [TS] and «disease perception» [DP]), – at baseline and 3-months follow-up. The enrolled sample was subdivided in a dichotomous manner into the HRQoL «improvement» or «non-improvement» patterns, based on the cut-off-values (COVs) of clinically meaningful change of the certain HRQoL parameter score at 3-months follow-up after PCI.Results and discussion. We revealed an improvement of average (median) HRQoL parameters at 3-months follow-up after PCI, namely PHsum (score increase from 38.8 to 43.1; р &lt; 0.001), SAQ-AS (25 to 75; р &lt; 0.001), SAQ-AF (70 to 80; р &lt; 0.001), SAQ-TS (58.8 to 70.6; р &lt; 0.001) and SAQ-DP (45.8 to 66.7; р &lt; 0.001). The clinically meaningful HRQoL improvement ranged from 14 % to 71 % cases, depending on the certain HRQoL parameter and the COVs of its change at follow-up after PCI. The worse baseline HRQoL, older age and higher baseline total cholesterol level were the factors, associated with the increased probability of HRQoL to be meaningfully improved after revascularization. In addition, a presence of diabetes mellitus, a history of acute cerebrovascular accident, and the ICA data on multivessel disease and in-stent restenosis after previous PCI, – all were associated with the lower odds of HRQoL «improvement» status to be achieved.Conclusions. A PCI favored the HRQoL improvement in SCAD patients at 3-months follow-up. The clinical and angiographic factors, associated with the post-procedure change in HRQoL, should be considered for a better selection of SCAD patients with intermediate coronary lesions for PCI.

Relationship between pan-immune- inflammation value and in major cardiovascular and cerebrovascular events in stable coronary artery disease patients undergoing on-pump coronary artery bypass graft surgery

BackgroundIn this study, we aimed to evaluate the association of pan-immune-inflammation value (PIV) with major cardiovascular and cerebrovascular events (MACCE) in stable coronary artery disease patients undergoing on-pump coronary artery bypass graft (CABG) surgery.MethodsWe retrospectively analyzed data from 527 patients who underwent on-pump CABG surgery for stable coronary artery disease between June 2015 and December 2020. Patients were categorized into two groups based on MACCE development. PIV levels were calculated from blood samples taken on admission. PIV was calculated as [neutrophil count (×103/µL)×platelet count (×103/µL))×monocyte count (×103/µL)]/lymphocyte count (×103/µL). The primary endpoint was long-term major cardiovascular and cerebrovascular events (MACCE) at a median follow-up of 4.6 years.ResultsOf the included patients, 103 (19.5%) developed MACCE. PIV was higher in patients with MACCE compared to those without (470.8 [295.3-606.8] vs. 269.8 [184.3-386.4], p < 0.001). Multivariate analysis showed a significant positive association between PIV and MACCE (HR: 1.326, 95%CI:1.212–1452, p < 0.001). The cut-off value for the PIV in the estimation of MACCE was 368.28 ( AUC: 0.726 with 69% sensitivity, 71% specificity, p < 0.001).ConclusionThis study shows a significant link between high PIV levels and MACCE in stable coronary artery disease patients undergoing on-pump CABG surgery. Our findings suggest that PIV may be a valuable, routinely available, and inexpensive marker for identifying patients at increased risk of MACCE.

The association between O2-pulse slope ratio and functional severity of coronary stenosis: A combined cardiopulmonary exercise testing and quantitative flow ratio study

BackgroundThe role of cardiopulmonary exercise testing (CPET) parameters in evaluating the functional severity of coronary disease remains unclear. The aim of this study was to quantify the O2-pulse morphology and investigate its relevance in predicting the functional severity of coronary stenosis, using Murray law-based quantitative flow ratio (μQFR) as the reference. MethodsCPET and μQFR were analyzed in 138 patients with stable coronary artery disease (CAD). The O2-pulse morphology was quantified through calculating the O2-pulse slope ratio. The presence of O2-pulse plateau was defined according to the best cutoff value of O2-pulse slope ratio for predicting μQFR ≤ 0.8. ResultsThe optimal cutoff value of O2-pulse slope ratio for predicting μQFR ≤ 0.8 was 0.4, with area under the curve (AUC) of 0.632 (95 % CI: 0.505–0.759, p = 0.032). The total discordance rate between O2-pulse slope ratio and μQFR was 27.5 %, with 13 patients (9.4 %) being classified as mismatch (O2-pulse slope ratio > 0.4 and μQFR ≤ 0.8) and 25 patients being classified as reverse-mismatch (O2-pulse slope ratio ≤ 0.4 and μQFR > 0.8). Angiography-derived microvascular resistance was independently associated with mismatch (OR 0.07; 95 % CI: 0.01–0.38, p = 0.002) and reverse-mismatch (OR 9.76; 95 % CI: 1.47–64.82, p = 0.018). ConclusionOur findings demonstrate the potential of the CPET-derived O2-pulse slope ratio for assessing myocardial ischemia in stable CAD patients.

Development and validation of a novel score for predicting perioperative major adverse cardiovascular events in patients with stable coronary artery disease undergoing noncardiac surgery

BackgroundA model developed specifically for stable coronary artery disease (SCAD) patients to predict perioperative major adverse cardiovascular events (MACE) has not been previously reported. MethodsThe derivation cohort consisted of 5780 patients with SCAD undergoing noncardiac surgery at the First Affiliated Hospital of Zhejiang University School of Medicine, from January 1, 2013 until May 31, 2021. The validation cohort consisted of 2677 similar patients from June 1, 2021 to May 31, 2023. The primary outcome was a composite of MACEs (death, resuscitated cardiac arrest, myocardial infarction, heart failure, and stroke) intraoperatively or during hospitalization postoperatively. ResultsSix predictors, including Creatinine >90 μmol/L, Hemoglobin <110 g/L, Albumin <40 g/L, Leukocyte >10 ×109/L, high-risk Surgery (general abdominal or vascular), and American Society of Anesthesiologists (ASA) class (III or IV), were selected in the final model (CHALSA score). Each patient was assigned a CHALSA score of 0, 1, 2, 3, or > 3 according to the number of predictors present. The incidence of perioperative MACEs increased steadily across the CHALSA score groups in both the derivation (0.5%, 1.4%, 2.9%, 6.8%, and 23.4%, respectively; p < 0.001) and validation (0.3%, 1.5%, 4.1%, 9.2%, and 29.2%, respectively; p < 0.001) cohorts. The CHALSA score had a higher discriminatory ability than the revised cardiac risk index (C statistic: 0.827 vs. 0.695 in the validation dataset; p < 0.001). ConclusionsThe CHALSA score showed good validity in an external dataset and will be a valuable bedside tool to guide the perioperative management of patients with SCAD undergoing noncardiac surgery.

Identification of Potential Crucial Biomarkers in STEMI Through Integrated Bioinformatic Analysis.

ST-segment elevation myocardial infarction (STEMI) is one of the leading causes of fatal cardiovascular diseases, which have been the prime cause of mortality worldwide. Diagnosis in the early phase would benefit clinical intervention and prognosis, but the exploration of the biomarkers of STEMI is still lacking. In this study, we conducted a bioinformatics analysis to identify potential crucial biomarkers in the progress of STEMI. We obtained GSE59867 for STEMI and stable coronary artery disease (SCAD) patients. Differentially expressed genes (DEGs) were screened with the threshold of |log2fold change| > 0.5 and p <0.05. Based on these genes, we conducted enrichment analysis to explore the potential relevance between genes and to screen hub genes. Subsequently, hub genes were analyzed to detect related miRNAs and DAVID to detect transcription factors for further analysis. Finally, GSE62646 was utilized to assess DEGs specificity, with genes demonstrating AUC results exceeding 75%, indicating their potential as candidate biomarkers. 133 DEGs between SCAD and STEMI were obtained. Then, the PPI network of DEGs was constructed using String and Cytoscape, and further analysis determined hub genes and 6 molecular complexes. Functional enrichment analysis of the DEGs suggests that pathways related to inflammation, metabolism, and immunity play a pivotal role in the progression from SCAD to STEMI. Besides, related-miRNAs were predicted, has-miR-124, has-miR-130a/b, and has-miR-301a/b regulated the expression of the largest number of genes. Meanwhile, Transcription factors analysis indicate that EVI1, AML1, GATA1, and PPARG are the most enriched gene. Finally, ROC curves demonstrate that MS4A3, KLRC4, KLRD1, AQP9, and CD14 exhibit both high sensitivity and specificity in predicting STEMI. This study revealed that immunity, metabolism, and inflammation are involved in the development of STEMI derived from SCAD, and 6 genes, including MS4A3, KLRC4, KLRD1, AQP9, CD14, and CCR1, could be employed as candidate biomarkers to STEMI.

Telomerase activity and hTERT gene expression in patients with acute coronary syndrome and stable coronary artery disease.

In this study, we aimed to examine the telomerase activity and hTERT gene expression in patients with acute coronary syndrome (ACS) and those with stable coronary artery disease (SCAD) and compare the results to controls. Additionally, we compared overall mortality rates relative to the telomerase activity. Atotal of 211 patients (78 ACS and 71 SCAD patients) were included in the study. The telomerase concentration was measured by ELISA and used to determine telomerase activity. The hTERT gene expression was determined by real-time PCR. The serum telomerase enzyme concentration was lower in ACS (36.61 ± 1.54) and SCAD (36.79 ± 1.57) when compared to the control group (37.03 ± 2.25). However, this difference did not reach statistical significance (p = 0.890). The hTERT gene expression acting in telomerase enzyme synthesis was 2.7-fold lower in ACS group (p = 0.070) and 2.2-fold lower in the SCAD group (p = 0.101) compared to the control group. Patients were followed for amedian of 32 months (minimum: 0.1, maximum: 46.8). The serum telomerase concentrations in patients who died and those survived in the SCAD group (35.98 ± 2.02 vs 36.86 ± 1.52 ng/ml, respectively; p= 0.529) were similar to those in the ACS group (36.39 ± 1.08 vs 36.63 ± 1.60 ng/ml, respectively p= 0.993). In the current study, telomerase activity or hTERT expression was similar in patients with ACS, SCAD, and controls. Moreover, telomerase activity was not associated with all- cause mortality during the 32-month follow-up (Tab. 3, Fig. 1, Ref. 29).

CLINICAL, ANGIOGRAPHIC AND FUNCTIONAL PARAMETERS DETERMINING DECISION TO PERFORM REVASCULARIZATION IN STABLE CORONARY ARTERY DISEASE PATIENTS WITH INTERMEDIATE CORONARY LESIONS

The aim: to study the clinical, angiographic and functional parameters, and their relation to the decision on percutaneous coronary intervention (PCI) in stable coronary artery disease (CAD) patients with intermediate coronary stenoses (ІСS) at patient and lesion levels.&#x0D; Materials and methods. The cross-sectional study enrolled 123 patients (62±9 years; 73,2 % males) with stable CAD and angiographically ICS (50-90 %). Stable angina CCS class II (CCSII) was diagnosed in 70 (56,9 %) patients, class III (CCSIII) – 29 (23,6 %); 24 (19,5 %) patients were free from angina (Afree). Fractional flow reserve (FFR) was assessed in 74 (60,2 %) patients (min per patient). The hemodynamically significant lesion was considered if FFR ≤0,80 a.u. The decision to perform PCI was undertaken in 93 (76 %) patients. In addition, the functional data from 128 lesions were analyzed.&#x0D; Results. The CCSIII group was characterized by less frequent previous PCI (21 % vs. 46 % in the pooled group [CCSII + Afree]; р=0,018); the predominance of cases with (max) severe [70-90 %] coronary stenosis (96 % vs. 78 % in CCSII and 54 % in Afree; ptrend&lt;0,001); the lower (min) FFR ([median, quartiles] 0,70 (0,64-0,74) vs. 0,87 (0,81-0,90) in Afree; p˂0,002); and the decision to perform PCI in the vast majority of cases (93 % vs. 79 % in CCSII and 46 % in Afree; ptrend&lt;0,001). The Afree/CCSII/CCSIII groups demonstrated a trend towards a decrease in frequency of cases with (max) [60-69 %] stenosis (38 %, 13 % and none, respectively; ptrend&lt;0,001), and a tendency towards the cases with (max) [80-90 %] stenosis to be more prevalent (29 %, 39 % and 55 %, respectively; ptrend=0,051). The frequency of cases with (max) stenosis [70-79 %] was comparable in the studied groups (Afree/CCSII/CCSIII: 25 %/39 %/41 %, respectively [ptrend=0,240]). At lesion-level, all [80-90 %] lesions (n=28) appeared to be hemodynamically significant. In turn, the [60-69 %] lesions (n=24) included 5 (21 %) significant ones. Finally, the [70-79 %] lesions (n=44) included 28 (64 %) significant and 16 (36 %) non-significant ones.&#x0D; Conclusions. Among the stable CAD patients with angiographically ICS, those with CCSIII were characterized by less frequent previous PCI, significant decrease in FFR and the decision to perform index PCI in the vast majority of cases. There is a need for more precise diagnosis and assessment of myocardial ischemia in patients with an intermediate pre-test obstructive CAD probability, including the cases of previously performed PCI.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) as a marker of coronary lesion severity in stable coronary artery disease (CAD) patients.

Coronary artery disease (CAD) remains a significant global health concern with considerable high morbidity and mortality and its development is influenced by various genetic and environmental factors. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a vital regulator of low-density lipoprotein receptor (LDLR) metabolism, directly impacting serum cholesterol levels. However, its role in development of CAD is not fully understood. The aim of this study was to assess the association between the level of PCSK9 and coronary lesion severity in patients with CAD. A case-control study using consecutive sampling was conducted among CAD patients at H. Adam Malik General Hospital and Murni Teguh Memorial Hospital, Medan, Indonesia. A total of 200 CAD patients were divided into two groups based on the SYNTAX score: control (score ≤22, n=100) and case (score >22, n=100). Plasma PCSK9 levels were measured from venous blood using quantitative sandwich enzyme immunoassay. The Chi-squared test was used to analyze the data. Our data suggested that PCSK9 level was associated with coronary lesion severity (p<0.001) of which high PCSK9 level was associated with severe coronary lesion. We also found that hypertension (p<0.001), smoking (p=0.072), diabetes (p<0.001), dyslipidemia (p<0.001), obesity (p=0.023), and family history (p=0.001) were associated with lesion severity. Using the receiver operating characteristic (ROC) curve analysis, the cut-off 70.35 ng/mL of PCSK9 had sensitivity 75% and specificity 78% to predict severe coronary lesion. This study highlights that PCSK9 level has moderate sensitivity and specificity to predict the coronary lesion severity among CAD patients.

A comprehensive proteomic profiling of urinary exosomes and the identification of early non-invasive biomarker in patients with coronary artery disease

Urinary small extracellular vesicles or exosomes (uEVs) source could be an emerging trove of biomarkers in coronary artery disease (CAD). It is a chronic inflammatory disease having a long asymptomatic phase of fatty-fibrous development in arteries leading to angina, myocardial infarction, and death. Our study was aimed at identifying differential protein expression profiling of uEVs in CAD. We collected urine samples of CAD patients (n = 41) age 18–65 years and gender matched healthy controls (n = 41). We isolated uEVs using differential ultracentrifugation. Further, uEV samples were characterized by western blotting exosome markers (Flotillin, TSG, CD63, and CD9), nano tracking analysis, and transmission and scanning electron microscopy. A total of 508 proteins were identified by iTRAQ-based mass spectrometry. We observed protein expression levels of AZGP1, SEMG1/2, ORM1, IGL, SERPINA5, HSPG2, prosaposin, gelsolin, and CD59 were upregulated, and UMOD, KNG1, AMBP, prothrombin, and TF were downregulated. Protein-protein interactions, gene ontology and pathway analysis were performed to functionally annotate identified uEVs proteins. A novel uEVs differential protein signature is shown. On validating UMOD protein by ELISA in two clinically different CAD, stable-CAD patients had lower levels than healthy controls whereas recent myocardial infarction patients had lowest. Our findings suggest UMOD importance as early diagnostic biomarker. SignificanceCoronary artery disease is a chronic inflammatory disease caused by gradual deposition of cholesterol and fat along with other proteins to develop plaque inside arteries. This further leads to blockage of artery, heart attack and death. There are no identifiable early biomarkers to diagnose this. For the first time, we have identified the differentially expressed proteins isolated from non-invasive uEV of CAD patients compared to healthy controls by using MS Orbitrap and iTRAQ labelling of peptides. We have identified decreased levels of UMOD protein in CAD. These findings have been confirmed by ELISA. Furthermore, the levels of UMOD were observed as more highly decreased in recent myocardial infarction CAD patients, indicating the importance of this protein as an early diagnostic biomarker. Conclusively, our study represents a non-invasive urinary EVs trove of differentially expressed proteins in CAD. This will form a groundwork for understanding the pathophysiology of CAD and will help in future translational research utilizing uEVs.

Feasibility and safety of left bundle branch area pacing for patients with stable coronary artery disease

AimsStable coronary artery disease (CAD) is a prevalent comorbidity among patients requiring pacemaker implantation. This comorbidity may have an impact on the safety and prognosis of traditional right ventricular pacing (RVP). Left bundle branch area pacing (LBBaP) is a new physiological pacing modality. Our aim was to investigate the feasibility and safety of LBBaP in patients with the stable CAD.MethodsThis study included 309 patients with symptomatic bradycardia who underwent LBBaP from September 2017 to October 2021. We included 104 patients with stable CAD (CAD group) and 205 patients without CAD (non-CAD group). Additionally, 153 stable CAD patients underwent RVP, and 64 stable CAD patients underwent His-bundle pacing (HBP) were also enrolled in this study. The safety and prognosis of LBBaP was assessed by comparing pacing parameters, procedure-related complications, and clinical events.ResultsDuring a follow-up period of 17.4 ± 5.3 months, the safety assessment revealed that the overall rates of procedure-related complications were similar between the stable CAD group and the non-CAD group (7.7% vs. 3.9%). Likewise, similar rates of heart failure hospitalization (HFH) (4.8% vs. 3.4%, stable CAD vs. non-CAD) and the primary composite outcome including death due to cardiovascular disease, HFH, or the necessity for upgrading to biventricular pacing (6.7% vs. 3.9%, stable CAD vs. non-CAD), were observed. In stable CAD patients, LBBaP demonstrated lower pacing thresholds and higher R wave amplitudes when compared to HBP. Additionally, LBBaP also had significantly lower occurrences of the primary composite outcome (6.7% vs. 19.6%, P = 0.003) and HFH (4.8% vs. 13.1%, P = 0.031) than RVP in stable CAD patients, particularly among patients with the higher ventricular pacing (VP) burden (&amp;gt;20% and &amp;gt;40%).ConclusionCompared with non-CAD patients, LBBaP was found to be attainable in stable CAD patients and exhibited comparable mid-term safety and prognosis. Furthermore, in the stable CAD population, LBBaP has demonstrated more stable pacing parameters than HBP, and better prognostic outcomes compared to RVP.

Computed tomography plaque analysis identifies residual inflammation in recent acute myocardial infarction patients

Abstract Introduction Residual inflammatory risk (RIR) following acute myocardial infarction (AMI) patients is associated with recurrent major adverse cardiovascular events. Atherosclerotic plaque quantification using computed tomographic coronary angiography (CTCA) can specifically identify inflamed plaque characteristics. We compared plaque burden and tissue composition in AMI patients with those of stable coronary artery disease (CAD) patients to identify imaging markers of RIR. Purpose We aimed to identify signs of residual inflammation in recent AMI patients via CTCA atheroma quantification. We hypothesised that recent AMI patients have plaque characteristics suggestive of inflammation. Methods 108 patients recruited from multiple sites with AMI &amp;lt;1 month were propensity-matched via CAD risk factors (age, gender, diabetes, hypertension, hyperlipidaemia, smoking and family history of CAD) with stable CAD patients in a 1:1 ratio. Propensity matched recent AMI and stable CAD patient cohorts had similar profiles: age (60±9.7 vs 57±10.0 years), gender (91.7% vs 92.6% male), diabetes (13.9% vs 15.7%), hypertension (44.4% vs 50.9%) and hyperlipidaemia (50.9% vs 63.9%, p&amp;gt;0.05 for all). Total plaque burden (total lesion volume/total vessel volume) and plaque composition (fibrous fatty [fibrofatty, FF, 31 – 130 HU], necrotic core [NC, -30 – 30 HU], fibrous [131 – 350 HU] and calcium [&amp;gt; 350 HU]) were extracted from CTCA scans and aggregated per patient. Culprit lesions of recent AMI patients were excluded from the analysis due to the fact that coronary stents would affect plaque characterisation. Multivariate linear regression, corrected for CAD risk factors, was used to compare these parameters between the two cohorts. Results Recent AMI patients and stable CAD patients had similar total plaque burden (β=0.001±0.013, p=0.950, Figure 1a). Patients with recent AMI had higher non-calcified plaque volume ratio (β=0.071±0.026, p&amp;lt;0.05, Figure 1b) due to higher FF (β=0.094±0.019, Figure 1d) and NC (β=0.025 ± 0.005, Figure 1e) plaque volume (p&amp;lt;0.05 for all), but less fibrous plaque volume (β = -0.048±0.019, p&amp;lt;0.05, Figure 1c). Conclusions Recent AMI patients had a greater non-calcified plaque burden than stable CAD patients due to larger FF and NC plaque burden. Since FF and NC components indicate ongoing inflammation in the plaque, while fibrous content indicates resolved inflammation; increased NC and FF burden suggest increased coronary plaque inflammation in non-culprit lesions of recent AMI patients, supporting the presence of residual inflammation in recent AMI patients.Figure 1

Health outcomes in patients with chronic coronary syndromes due to obstructive or non-obstructive coronary arteries

Abstract Background Angina is the clinical hallmark of myocardial ischaemia and often arises from obstructive coronary artery disease (diagnosed as stable CAD), for which there are established guideline therapies. However, when coronary angiography does not reveal obstructive CAD (i.e. &amp;lt;50% stenoses), the management pathway for these patients with Angina with Non-Obstructive Coronary Arteries (ANOCA) is less clear. Purpose To compare the clinical characteristics and outcomes of patients with Stable CAD vs. ANOCA, who were referred to invasive angiography for the assessment of angina. Methods Consecutive angina patients undergoing elective coronary angiography enrolled in the CADOSA (Coronary Angiogram Database of South Australia) Registry between 2012-2018 were included. In-hospital clinical data was extracted from CADOSA and mortality and hospitalisation data over 3 years was extracted via administrative records. Results Among 30,015 angiograms performed, there were 2,245 ANOCA (&amp;lt;50% stenosis), and 4,131 Stable CAD (≥50% stenosis) patients. ANOCA patients were younger (61±11 vs 66±11, p&amp;lt;0.05) and more often female (59% vs 27%, p&amp;lt;0.05) compared to Stable CAD. ANOCA and Stable CAD patients were indistinguishable in relation to (i) chest pain quality (tightness, 42% vs 41%, p&amp;gt;0.05) (ii) chest pain precipitant (exertion, 60% vs 65%, p&amp;lt;0.05), (iii) relieving factors (nitrates 20% vs 22%, p&amp;gt;0.05). Further, the frequency of non-invasive ischaemia test prior to angiography (64% vs 62%, p&amp;lt;0.05) and objective evidence of ischaemia (70% vs 77%, p&amp;gt;0.05) was similar between ANOCA and Stable CAD. In contrast, discharge therapies differed markedly between ANOCA and Stable CAD patients in (i) cardioprotective agents (81% vs 96%, respectively), and (ii) anti-ischaemic agents (75% vs 90%, respectively), all p&amp;lt;0.05. Only 6% of ANOCA patients received further cardiac investigation whereas revascularisation was undertaken in 35% of the Stable CAD cohort. All-cause mortality at 3 years was higher in Stable CAD patients compared to ANOCA (3% vs 2%, p&amp;lt;0.05). There were frequent return hospital visits for chest pain in both Stable CAD and ANOCA patients over 3 years including (i) emergency presentation (24% vs 18%, respectively) and (ii) hospital admission (18% vs 11%, respectively), all p&amp;lt;0.05. Conclusion Prior to angiography, the chest pain features, and non-invasive ischaemic markers are indistinguishable in ANOCA and Stable CAD patients. However, following angiography, Stable CAD patients receive an appropriate diagnosis and guideline therapy. In contrast, the ANOCA patients (a) seldom receive additional investigation to identify the underlying angina mechanisms, (b) are less often prescribed cardioprotective and anti-anginal agents, (c) yet often experience recurrent symptoms. This study underscores the need to focus improvement on diagnostic work-up for ANOCA and therapies targeted at managing symptoms.

Bailout inclisiran-based triple lipid-lowering therapy reduces plaque lipid content in stable coronary artery disease patients

Abstract Background Low-density lipoprotein cholesterol (LDL-C) has a causal role in atherosclerotic cardiovascular disease. Genetic studies and variability in individual response to lipid-lowering therapies suggest combining hypolipidaemic medications with different mechanisms of action. Purpose The aim of this study was to evaluate the effect of triple inclisiran-based hypolipidaemic therapy in patients not reaching LDL-C target on maximum statin/ezetimibe treatment. Methods This prospective study enrolled 37 stable coronary artery disease patients admitted for elective percutaneous coronary intervention after 4-6 weeks on maximum tolerated statin and/or ezetimibe therapy during run-in period. Afterwards, patients with LDL-C level &amp;gt;1.8 mmol/l at the time of inclusion were assigned to receive add-on inclisiran (triple therapy group). In all participants near-infrared spectroscopy (NIRS) was performed at baseline and after 15 months for atherosclerotic plaque evaluation in the segment of interest, defined as 20-50% lesion in the proximal or middle third of a coronary artery. Statistical analysis was carried out with SPSS Statistics software. Results Average LDL-C level among screened patients was 2.81 (±1.17) mmol/l. In 19 patients LDL-C level remained &amp;gt;1.8 mmol/l on maximally tolerated statin and/or ezetimibe treatment, and after 15 months of triple therapy mean LDL-C reached 1.81 (±1.02) mmol/l with a significant LDL-C percentage change of 35.59% (95%CI -47.31 to -9.18, P=0.006) in this group. 17 patients continued statin/ezetimibe as mono or dual treatment and at 15-month follow-up mean LDL-C level comprised 1.67 (±0.61) mmol/l among these participants. According to NIRS data, maximum lipid-core burden index within 4 mm (maxLCBI4 mm) was significantly reduced by 28.85 (95%CI -189.39 to 17.64, P=0.041) in triple therapy group and by 114.72 in mono or dual therapy group (-194.76 to 23.01, P=0.004), with no statistically significant difference established between both groups (P=0.494). Conclusions Triple therapy demonstrated significant atherosclerotic plaque lipid content reduction along with LDL-C level lowering in patients with insufficient effectiveness of statin/ezetimibe treatment.

Association between high-intensity lipid-lowering therapy and atherosclerotic plaque content changes assed by iMAP-IVUS and near-infrared spectroscopy in patients with premature atherosclerosis

Abstract Background/Introduction The benefits of lipid-lowering drug treatment for the secondary prevention of coronary heart disease have been well-established by randomized, controlled trials. More evidence has now emerged to support the use of high-intensity low-density lipoprotein cholesterol (LDL-C) –lowering therapy including statine, ezetimibe, and PCSK9 inhibitors. Intravascular imaging, such as near-infrared spectroscopy (NIRS) can detect lipid-rich plaques. Virtual histology iMAP-Intravascular ultrasound (iMAP-IVUS) can classify tissue characteristics into 4 major components fibrotic, lipidic, necrotic, and calcified. Purpose Our study aimed to evaluate atherosclerotic plaque composition in very high cardiovascular-risk patients, who received high-intensity lipid-lowering therapy for 15 months. Methods Our study included stable coronary artery disease patients receiving statin and/or ezetimibe in maximum tolerated dose for at least one month, who were scheduled for PCI. In case LDL-C was &amp;gt;1.8 mmol/l, inclisiran was added to the therapy at the time of inclusion and continued for 15 months. The region of interest was a proximal or middle segment with angiographic evidence of nonobstructive de novo atherosclerosis &amp;gt;20% and &amp;lt;50%, evaluated by NIRS and iMAP-IVUS at baseline and 15 months later. After 15 months patients were classified into two groups – those who reached the European Society of Cardiology LDL-C target &amp;lt;1.8 mmol/L and those who did not. Statistical analysis was carried out with SPSS Statistics software, defining a significance level of 0.05. Results 37 eligible patients had undergone IVUS/NIRS investigation. The mean patient age was 53 years. After 15 months the mean LDL-C level decreased from 2.70 mmol/L to 1.79 mmol/l and 25 patients reached a target of &amp;lt;1.8 mmol/L. In the patient group that reached target - 4mm plaque lipid core burden index (LCBImax4mm) decreased from 184.00 (±160.07) to 62.72 (±142.19) with p=0.001 and total LCBI changed from 37.04 (± 40.80) to 15.60 (± 27.87) with p = 0.007. In patients with LDL-C &amp;gt;1.8 mmol/L, LCBImax4mm changed from 211.16 (±167.76) to 125.04 (±152.21) with no statistically significant difference p = 0.074. Similarly, the total LCBI was from 40.33 (± 43.38) to 22.41 (± 24.97) with p = 0.086. In iMAP-IVUS results necro-lipidic core in the &amp;lt;1.8 mmol/L group changed from 78.50 mm3 (±42.77) to 84.77 mm3 (±46.03) p = 0.422. Yet, second group's necro-lipidic core changed from 97.43 mm3 (±58.04) to 89.40 mm3 (±49.03), with no statistically significant difference p = 0.066. Additionally in both groups were significant changes in fibrotic tissues, for the target group from 139.50 mm3 (±69.86) to 147.32 mm3 (±73.56) p = 0.002 and from 149.71 mm3 (±82.79) to 160.09 mm3 (±89.01) p = 0.008 in second group. Conclusion Our study showed that after 15 months of high-intensity lipid-lowering therapy, patients that reached LDL-C levels &amp;lt;1.8 mmol/L, showed lower LCBImax4mm and total LCBI.

Abstract 15419: Adiponectin’s Predictive Role in Long-Term Mortality and Major Adverse Cardiovascular Events in Patients With Stable Coronary Artery Disease: A Meta-Analysis of Prospective Studies

INTRODUCTION: The relentless toll of cardiovascular disease in the United States demands a breakthrough in reliable and cost-effective prognostic markers. Amidst the limited knowledge surrounding the role of adiponectin in stable coronary artery disease (CAD), this study aims to unveil its power in predicting all-cause mortality and major adverse cardiovascular events (MACE) among patients with stable coronary artery disease (CAD). METHODS: We systematically screened PubMed, Scopus, and Google Scholar for articles until May 2023 to identify relevant studies. Random-effects model estimated the pooled odds ratio (OR) with 95% confidence intervals (CI), and I2 statistics assessed heterogeneity. The leave-one-out method was used for sensitivity analysis. RESULTS: Following the screening, five prospective studies involving 3225 patients with a median follow-up duration of 3.8 years were included. In the study population, hypertension, diabetes, hyperlipidemia, and smoking were prevalent risk factors, and common medications included angiotensin-converting enzyme inhibitors, beta-blockers, and statins. The pooled adjusted OR for all-cause mortality was 2.51 (95%CI: 1.36-4.62), with moderate heterogeneity (I2=65.51%, p=0.03), and the pooled adjusted OR for MACE was 1.04 (95%CI: 1.02-1.06), with no significant heterogeneity (I2=0%, p=0.68) (Fig. 1) . The leave-one-out sensitivity analysis showed that no single study significantly influenced the meta-analysis results, indicating robustness. CONCLUSION: Higher adiponectin levels were associated with higher odds of long-term mortality and MACE in stable CAD patients, highlighting its potential as a cost-effective marker for risk stratification and guiding management strategies. Further studies exploring the role of adiponectin can significantly impact clinical decision-making and resource allocation in cardiovascular care.

Abstract 13473: 3D Fusion Between SPECT Myocardial Perfusion Imaging and Invasive Coronary Angiography to Guide Revascularization in Patients With Stable Coronary Artery Disease

Objective: We evaluated the value of 3-dimensional (3D) fusion of SPECT myocardial perfusion imaging (MPI) with invasive coronary angiography (ICA) to guide revascularization. Methods: A retrospective observational study of 621 patients who underwent SPECT MPI and ICA. Based on the location of perfusion defect and stenosis on ICA, patients were classified into matched, unmatched, or normal groups via 3D fusion. The concordance between treatments was defined as, matched if there was revascularization in concordance with 3D fusion recommendation or if patient did not require revascularization; otherwise, they were classified as discordant. Major adverse cardiac events (MACE) (cardiac death, myocardial infarction, unstable angina requiring hospitalization or ICA, and unplanned revascularization) after revascularization of lesion recommended by 3D fusion were compared with those that the patients actually received. Results: Over a five-year follow-up period, 16% experienced MACE. Rates of MACE were 69% for matched findings, 22% for unmatched findings, 9% for normal findings (P&lt;0.01). Among the 366 patients who had at least one vessel with a stenosis of &gt;=50%, those whose treatments were concordant with the fusion had significantly better outcomes compared to those who were not (P&lt;0.05), primarily observed in the intermediate stenosis group (stenosis: 50-79%) (P&lt;0.01) (Fig. A). Further, in the intermediate stenosis patients, the revascularization ratio in the concordant group was significantly higher in the LCX (31.2% vs. 14.3%, P&lt;0.01) than that in the discordant group. (Fig. B) Conclusions: 3D fusion prior to coronary revascularization can guide coronary revascularization to improve outcomes, among patients with stable CAD patients and intermediate stenosis.

Abstract 17772: The Relationship Between Renin-Angiotensin System Inhibition and Coronary Artery Calcification Evaluated by Intravascular Ultrasound

Introduction: Coronary artery calcification is significantly associated with major adverse cardiac events in patients with coronary artery disease (CAD), and severely calcified lesions are significantly associated with poor outcomes after percutaneous coronary intervention (PCI). Hypothesis: The relationship between renin-angiotensin system inhibition and coronary artery calcification is unknown. Methods: Five hundred stable CAD patients undergoing PCI were divided into none/mild and moderate/severe calcification groups according to the grade of calcification in the target lesion evaluated by intravascular ultrasound (IVUS). Calcification with a calcium arch &amp;gt;180° and calcium length &amp;gt;5 mm in the target lesion was defined as moderate/severe calcification. We examined the association between patient’s characteristics and morphology in target lesions assessed by IVUS. Results: One hundred ninety of the 500 patients (38%) showed moderate/severe calcification of the culprit lesion. In the moderate/severe calcification group, the survival rate was significantly lower, and cumulative incidence of major cardiovascular and cerebrovascular events (MACCE) was higher than in the none/mild calcification group after PCI (p=0.015 and p=0.003, respectively). Age, body mass index, hypertension, use of angiotensin-converting enzyme inhibitor (ACEI), hemodialysis, high-sensitivity C-reactive protein levels, low-density lipoprotein cholesterol levels, serum albumin levels were associated with moderate/severe calcification lesion in univariate logistic analysis, but the use of angiotensin II receptor blocker was not. Multivariate logistic analysis identified age [odds ratio (OR); 1.05, 95% confidence interval (CI): 1.02-1.08, p&amp;lt;0.001], use of ACEI (OR; 0.46, 95% CI: 0.23-0.91, p=0.025), and hemodialysis (OR; 6.07, 95% CI: 2.39-15.42, p&amp;lt;0.001) as independent factors of moderate/severe calcification lesions. A comparison of P-value for interaction of use of ACEI and hemodialysis was p=0.51. Conclusions: Using of ACEI was negatively associated with moderate/severe calcification in target lesions assessed by IVUS. ACEI may have a potential for inhibitory effect on coronary artery calcification.